tbuckley/cabot-search huggingface dataset:
Early switch to oral antibiotic therapy in patients with low-risk neutropenic sepsis (EASI-SWITCH): a randomized non-inferiority trial
Authors: Vicky Coyle, Caroline Forde, Danny F. McAuley, Richard H. Wilson, Mike Clarke, Ruth Plummer, Margaret Grayson, Cliona McDowell, Ashley Agus, Annmarie Doran, Anne L. Thomas, Rosemary A. Barnes, Richard Adams, Ian Chau, Dawn Storey, Ronan McMullan
Journal: Clinical Microbiology and Infection (2023)

<h2>Abstract</h2><h3>Objectives</h3> To determine whether early switch to oral antibiotic treatment in adults with neutropenic sepsis at low risk of complications, is non-inferior to switching later. <h3>Methods</h3> This non-inferiority, parallel group, randomized, open-label clinical trial enrolled UK adults hospitalized with neutropenic sepsis. Participants were randomly assigned to either switch to oral ciprofloxacin plus co-amoxiclav within 12-24 hours or to continue intravenous treatment for at least 48 hours. The primary outcome was a composite measure of treatment failure, 14 days after randomization. The non-inferiority margin was 15%. <h3>Results</h3> There were 129 participants from 16 centres and 125 were assessed for the primary outcome. Of these, 113 patients completed protocolized treatment and comprised the per protocol population. In total, 9 of 64 patients (14·1%) in the standard care arm met the primary endpoint, compared with 15 of 61 (24.6%) in the early switch arm, giving a risk difference of 10·5% (1-sided 95% CI, -∞% to 22%; P=0·14). In the per protocol population, 8 of the 60 patients (13·3%) in the standard care arm met the primary endpoint, compared with 9 of 53 (17%) in the intervention arm giving a risk difference of 3·7% (1-sided 95% CI, -∞% to 14·8%; P=0·59). Duration of hospital stay was shorter in the intervention arm (median 2 [IQR 2,3] vs. 3 days [IQR 2,4]; P=0·002). <h3>Conclusion</h3> While non-inferiority of early oral switch was found in the per protocol population, the intervention was not non-inferior in the intent to treat population.
Snoopligase-catalyzed molecular glue enables efficient generation of hyperoligomerized TRAIL variant with enhanced antitumor effect
Authors: Tianshan She, Fen Yang, Shiyuan Chen, Hao Yang, Ze Tao, Huimin Xing, Jie Chen, Huansheng Chang, Hongyu Lu, Tao Su, Youmei Jin, Yi Zhong, Jingqiu Cheng, Hong Zhu, Xiaofeng Lu
Journal: Journal of Controlled Release (2023)
Targeting proteostasis network in osteoporosis: Pathological mechanisms and therapeutic implications
Authors: Cong Ma, Ronghui Yu, Junhong Li, Jiashuo Chao, Ping Liu
Journal: Ageing Research Reviews (2023)

As the most common bone disease, osteoporosis (OP) increases bone fragility and makes patients more vulnerable to the threat of osteoporotic fractures. With the ageing population in today's society, OP has become a huge and growing public health problem. Unfortunately, the clear pathogenesis of OP is still under exploration, and effective interventions are still scarce. Therefore, exploring new targets for pharmacological interventions to develop promising therapeutic drugs for OP is of great clinical value. Previous studies have shown that normal bone remodeling depends on proteostasis, whereas loss of proteostasis during ageing leads to the dysfunctional proteostasis network (PN) that fails to maintain bone homeostasis. Nevertheless, only a few studies have revealed the pathophysiological relationship between bone metabolism and a single component of PN, yet the role of PN as a whole in the pathogenesis of OP is still under investigation. This review comprehensively summarized the role of PN in the pathogenesis of OP and further discussed the potential of PN as innovative drug targets for the therapy of OP.
HlyF, an underestimated virulence factor of uropathogenic Escherichia coli
Authors: Camille V. Chagneau, Delphine Payros, Audrey Goman, Cécile Goursat, Laure David, Miki Okuno, Pierre-Jean Bordignon, Carine Séguy, Clémence Massip, Priscilla Branchu, Yoshitoshi Ogura, Jean-Philippe Nougayrède, Marc Marenda, Eric Oswald
Journal: Clinical Microbiology and Infection (2023)
Aortic valve calcification is promoted by interleukin-8 and restricted through antagonizing CXC motif chemokine receptor 2
Authors: Kawthar Dhayni, Yuthiline Chabry, Lucie Hénaut, Carine Avondo, Cedric Boudot, Hakim Ouled-Haddou, Edith Bigot-Corbel, Gilles Touati, Thierry Caus, Hind Messaoudi, Jérémy Bellien, Christophe Tribouilloy, David Messika-Zeitoun, Kazem Zibara, Saïd Kamel, Youssef Bennis
Journal: Cardiovascular Research (2023)

Inflammatory cytokines play a critical role in the progression of calcific aortic valve disease (CAVD), for which there is currently no pharmacological treatment. The aim of this study was to test the hypothesis that interleukin-8 (IL-8), known to be involved in arterial calcification, also promotes aortic valve calcification (AVC) and to evaluate whether pharmacologically blocking the IL-8 receptor, CXC motif chemokine receptor 2 (CXCR2), could be effective in preventing AVC progression.A cohort of 195 patients (median age 73, 74% men) diagnosed with aortic valve stenosis (severe in 16.9% of cases) were prospectively followed by CT for a median time of 2.6 years. A Cox proportional hazards regression analysis indicated that baseline IL-8 serum concentrations were associated with rapid progression of AVC, defined as an annualized change in the calcification score by CT ≥ 110 AU/year, after adjustment for age, gender, bicuspid anatomy, and baseline disease severity. In vitro, exposure of primary human aortic valvular interstitial cells (hVICs) to 15 pg/mL IL-8 induced a two-fold increase in inorganic phosphate (Pi)-induced calcification. IL-8 promoted NFκB pathway activation, MMP-12 expression, and elastin degradation in hVICs exposed to Pi. These effects were prevented by SCH527123, an antagonist of CXCR2. The expression of CXCR2 was confirmed in hVICs and samples of aortic valves isolated from patients with CAVD, in which the receptor was mainly found in calcified areas, along with MMP-12 and a degraded form of elastin. Finally, in a rat model of chronic kidney disease-associated CAVD, SCH527123 treatment (1 mg/kg/day given orally for 11 weeks) limited the decrease in aortic cusp separation, the increase in maximal velocity of the transaortic jet, and the increase in aortic mean pressure gradient measured by echocardiography, effects that were associated with a reduction in hydroxyapatite deposition and MMP-12 expression in the aortic valves.Overall, these results highlight, for the first time, a significant role for IL-8 in the progression of CAVD by promoting calcification via a CXCR2- and MMP-12-dependent mechanism that leads to elastin degradation, and identify CXCR2 as a promising therapeutic target for the treatment of CAVD.
E-cigarettes and arrhythmogenesis: a comprehensive review of pre-clinical studies and their clinical implications
Authors: Carson A Jones, Michael J Wallace, Priya Bandaru, Emerson D Woodbury, Peter J Mohler, Loren E Wold
Journal: Cardiovascular Research (2023)

Abstract Electronic cigarette use has grown exponentially in recent years, and while their popularity has increased, the long-term effects on the heart are yet to be fully studied and understood. Originally designed as devices to assist with those trying to quit traditional combustible cigarette use, their popularity has attracted use by teens and adolescents who traditionally have not smoked combustible cigarettes. Acute effects on the heart have been shown to be similar to traditional combustible cigarettes, including increased heart rate and blood pressure. The main components of electronic cigarettes that contribute to these arrhythmic effects are found in the e-liquid that is aerosolized and inhaled, comprised of nicotine, flavourings, and a combination of vegetable glycerin (VG) and propylene glycol (PG). Nicotine can potentially induce both ventricular and atrial arrhythmogenesis, with both the atrial and ventricular effects resulting from the interactions of nicotine and the catecholamines they release via potassium channels. Atrial arrhythmogenesis, more specifically atrial fibrillation, can also occur due to structural alterations, which happens because of nicotine downregulating microRNAs 133 and 590, both post-transcriptional growth factor repressors. Liquid flavourings and the combination of PG and VG can possibly lead to arrhythmic events by exposing users to acrolein, an aldehyde that stimulates TRPA1 that in turn causes a change towards sympathetic activation and autonomic imbalance. The design of these electronic delivery devices is constantly changing; therefore, it has proven extremely difficult to study the long-term effects on the heart caused by electronic cigarettes but will be important to understand given their rising popularity. The arrhythmic effects of electronic cigarettes appear similar to traditional cigarettes as well; however, a comprehensive review has not been compiled and is the focus of this article.
Microfluidic intestinal organoid-on-a-chip uncovers therapeutic targets by recapitulating oxygen dynamics of intestinal IR injury
Authors: Jinjian Huang, Ziyan Xu, Jiao Jiao, Zongan Li, Sicheng Li, Ye Liu, Ze Li, Guiwen Qu, Jie Wu, Yun Zhao, Kang Chen, Jieshou Li, Yichang Pan, Xiuwen Wu, Jianan Ren
Journal: Bioactive Materials (2023)

Increasing evidence demonstrates that mammals have different reactions to hypoxia with varied oxygen dynamic patterns. It takes ∼24 h for tri-gas incubator to achieve steady cell hypoxia, which fails to recapitulate ultrafast oxygen dynamics of intestinal ischemia/reperfusion (IR) injury. Inspired from the structure of native intestinal villi, we engineered an intestinal organoid chip embedded with engineered artificial microvessels based on co-axial microfluidic technology by using pH-responsive ZIF-8/sodium alginate scaffold. The chip was featured on: (i) eight times the oxygen exchange efficiency compared with the conventional device, tri-gas incubator, (ii) implantation of intestinal organoid reproducing all types of intestinal epithelial cells, and (iii) bio-responsiveness to hypoxia and reoxygenation (HR) by presenting metabolism disorder, inflammatory reaction, and cell apoptosis. Strikingly, it was found for the first time that Olfactomedin 4 (Olfm4) was the most significantly down-regulated gene under a rapid HR condition by sequencing the RNA from the organoids. Mechanistically, OLFM4 played protective functions on HR-induced cell inflammation and tissue damage by inhibiting the NF-kappa B signaling activation, thus it could be used as a therapeutic target. Altogether, this study overcomes the issue of mismatched oxygen dynamics between in vitro and in vivo, and sets an example of next-generation multisystem-interactive organoid chip for finding precise therapeutic targets of IR injury.
Plasma Membrane Channel TRPM4 Mediates Immunogenic Therapy–Induced Necrosis
Authors: Santanu Ghosh, Rachel Yang, Darjan Duraki, Junyao Zhu, Ji Eun Kim, Musarrat Jabeen, Chengjian Mao, Xinyi Dai, Mara R. Livezey, Matthew W. Boudreau, Ben H. Park, Erik R. Nelson, Paul J. Hergenrother, David J. Shapiro
Journal: Cancer Research (2023)

Several emerging therapies kill cancer cells primarily by inducing necrosis. As necrosis activates immune cells, potentially, uncovering the molecular drivers of anticancer therapy-induced necrosis could reveal approaches for enhancing immunotherapy efficacy. To identify necrosis-associated genes, we performed a genome-wide CRISPR-Cas9 screen with negative selection against necrosis-inducing preclinical agents BHPI and conducted follow-on experiments with ErSO. The screen identified transient receptor potential melastatin member 4 (TRPM4), a calcium-activated, ATP-inhibited, sodium-selective plasma membrane channel. Cancer cells selected for resistance to BHPI and ErSO exhibited robust TRPM4 downregulation, and TRPM4 reexpression restored sensitivity to ErSO. Notably, TRPM4 knockout (TKO) abolished ErSO-induced regression of breast tumors in mice. Supporting a broad role for TRPM4 in necrosis, knockout of TRPM4 reversed cell death induced by four additional diverse necrosis-inducing cancer therapies. ErSO induced anticipatory unfolded protein response (a-UPR) hyperactivation, long-term necrotic cell death, and release of damage-associated molecular patterns that activated macrophages and increased monocyte migration, all of which was abolished by TKO. Furthermore, loss of TRPM4 suppressed the ErSO-induced increase in cell volume and depletion of ATP. These data suggest that ErSO triggers initial activation of the a-UPR but that it is TRPM4-mediated sodium influx and cell swelling, resulting in osmotic stress, which sustains and propagates lethal a-UPR hyperactivation. Thus, TRPM4 plays a pivotal role in sustaining lethal a-UPR hyperactivation that mediates the anticancer activity of diverse necrosis-inducing therapies.
Pediatric Hospitalizations and ICU Admissions Due to COVID-19 and Pediatric Inflammatory Multisystem Syndrome Temporally Associated With SARS-CoV-2 in England
Authors: Joseph L. Ward, Rachel Harwood, Simon Kenny, Joana Cruz, Matthew Clark, Peter J. Davis, Elizabeth S. Draper, Dougal Hargreaves, Shamez N. Ladhani, Nick Gent, Hannah E. Williams, Karen Luyt, Steve Turner, Elizabeth Whittaker, Alex Bottle, Lorna K. Fraser, Russell M. Viner
Journal: JAMA Pediatrics (2023)

Investigating how the risk of serious illness after SARS-CoV-2 infection in children and adolescents has changed as new variants have emerged is essential to inform public health interventions and clinical guidance.
Machine learning‐based prediction of in‐hospital death for patients with takotsubo syndrome: The <scp>InterTAK‐ML</scp> model
Authors: Ovidio De Filippo, Victoria L. Cammann, Corrado Pancotti, Davide Di Vece, Angelo Silverio, Victor Schweiger, David Niederseer, Konrad A. Szawan, Michael Würdinger, Iva Koleva, Veronica Dusi, Michele Bellino, Carmine Vecchione, Guido Parodi, Eduardo Bossone, Sebastiano Gili, Michael Neuhaus, Jennifer Franke, Benjamin Meder, Miłosz Jaguszewski, Michel Noutsias, Maike Knorr, Thomas Jansen, Wolfgang Dichtl, Dirk von Lewinski, Christof Burgdorf, Behrouz Kherad, Carsten Tschöpe, Annahita Sarcon, Jerold Shinbane, Lawrence Rajan, Guido Michels, Roman Pfister, Alessandro Cuneo, Claudius Jacobshagen, Mahir Karakas, Wolfgang Koenig, Alexander Pott, Philippe Meyer, Marco Roffi, Adrian Banning, Mathias Wolfrum, Florim Cuculi, Richard Kobza, Thomas A. Fischer, Tuija Vasankari, K.E. Juhani Airaksinen, L. Christian Napp, Rafal Dworakowski, Philip MacCarthy, Christoph Kaiser, Stefan Osswald, Leonarda Galiuto, Christina Chan, Paul Bridgman, Daniel Beug, Clément Delmas, Olivier Lairez, Ekaterina Gilyarova, Alexandra Shilova, Mikhail Gilyarov, Ibrahim El‐Battrawy, Ibrahim Akin, Karolina Poledniková, Petr Toušek, David E. Winchester, Michael Massoomi, Jan Galuszka, Christian Ukena, Gregor Poglajen, Pedro Carrilho‐Ferreira, Christian Hauck, Carla Paolini, Claudio Bilato, Yoshio Kobayashi, Ken Kato, Iwao Ishibashi, Toshiharu Himi, Jehangir Din, Ali Al‐Shammari, Abhiram Prasad, Charanjit S. Rihal, Kan Liu, P. Christian Schulze, Matteo Bianco, Lucas Jörg, Hans Rickli, Gonçalo Pestana, Thanh H. Nguyen, Michael Böhm, Lars S. Maier, Fausto J. Pinto, Petr Widimský, Stephan B. Felix, Ruediger C. Braun‐Dullaeus, Wolfgang Rottbauer, Gerd Hasenfuß, Burkert M. Pieske, Heribert Schunkert, Monika Budnik, Grzegorz Opolski, Holger Thiele, Johann Bauersachs, John D. Horowitz, Carlo Di Mario, Francesco Bruno, William Kong, Mayank Dalakoti, Yoichi Imori, Thomas Münzel, Filippo Crea, Thomas F. Lüscher, Jeroen J. Bax, Frank Ruschitzka, Gaetano Maria De Ferrari, Piero Fariselli, Jelena R. Ghadri, Rodolfo Citro, Fabrizio D'Ascenzo, Christian Templin
Journal: European Journal of Heart Failure (2023)

Takotsubo syndrome (TTS) is associated with a substantial rate of adverse events. We sought to design a machine learning (ML)-based model to predict the risk of in-hospital death and to perform a clustering of TTS patients to identify different risk profiles.
Phase I Trial of the Multi-kinase Inhibitor Cabozantinib, a CYP3A4 Substrate, plus CYP3A4-Interacting Antiretroviral Therapy in People Living with HIV and Cancer (AMC-087)
Authors: Missak Haigentz, Jeannette Y. Lee, Elizabeth Y. Chiao, David M. Aboulafia, Lee Ratner, Richard F. Ambinder, Robert A. Baiocchi, Ronald T. Mitsuyasu, William Wachsman, Joseph A. Sparano, Michelle A. Rudek
Journal: Clinical Cancer Research (2023)

To evaluate the safety, pharmacokinetics, and pharmacodynamic effects of cabozantinib, a CYP3A4 substrate, in people living with human immunodeficiency virus and cancer receiving antiretrovirals (ARV).
COVID-19 in Children—Learning From the Past, Planning for the Future
Authors: Kathleen Chiotos, Julie C. Fitzgerald
Journal: JAMA Pediatrics (2023)

Joseph L. Ward, PhD; Rachel Harwood, PhD; Simon Kenny, MD; Joana Cruz, PhD; Matthew Clark, MB, BChir; Peter J. Davis, MB, ChB; Elizabeth S. Draper, PhD; Dougal Hargreaves, MD (Res); Shamez N. Ladhani, PhD; Nick Gent, MB, ChB; Hannah E. Williams, PhD; Karen Luyt, PhD; Steve Turner, MD; Elizabeth Whittaker, PhD; Alex Bottle, PhD; Lorna K. Fraser, PhD; Russell M. Viner, PhD
At-Risk Genomic Findings for Pediatric-Onset Disorders From Genome Sequencing vs Medically Actionable Gene Panel in Proactive Screening of Newborns and Children
Authors: Jorune Balciuniene, Ruby Liu, Lora Bean, Fen Guo, Babi Ramesh Reddy Nallamilli, Naga Guruju, Xiangwen Chen-Deutsch, Rizwan Yousaf, Kristina Fura, Ephrem Chin, Abhinav Mathur, Zeqiang Ma, Jonathan Carmichael, Cristina da Silva, Christin Collins, Madhuri Hegde
Journal: JAMA Network Open (2023)

Although the clinical utility of genome sequencing for critically ill children is well recognized, its utility for proactive pediatric screening is not well explored.To evaluate molecular findings from screening ostensibly healthy children with genome sequencing compared with a gene panel for medically actionable pediatric conditions.This case series study was conducted among consecutive, apparently healthy children undergoing proactive genetic screening for pediatric disorders by genome sequencing (n = 562) or an exome-based panel of 268 genes (n = 606) from March 1, 2018, through July 31, 2022.Genetic screening for pediatric-onset disorders using genome sequencing or an exome-based panel of 268 genes.Molecular findings indicative of genetic disease risk.Of 562 apparently healthy children (286 girls [50.9%]; median age, 29 days [IQR, 9-117 days]) undergoing screening by genome sequencing, 46 (8.2%; 95% CI, 5.9%-10.5%) were found to be at risk for pediatric-onset disease, including 22 children (3.9%) at risk for high-penetrance disorders. Sequence analysis uncovered molecular diagnoses among 32 individuals (5.7%), while copy number variant analysis uncovered molecular diagnoses among 14 individuals (2.5%), including 4 individuals (0.7%) with chromosome scale abnormalities. Overall, there were 47 molecular diagnoses, with 1 individual receiving 2 diagnoses; of the 47 potential diagnoses, 22 (46.8%) were associated with high-penetrance conditions. Pathogenic variants in medically actionable pediatric genes were found in 6 individuals (1.1%), constituting 12.8% (6 of 47) of all diagnoses. At least 1 pharmacogenomic variant was reported for 89.0% (500 of 562) of the cohort. In contrast, of 606 children (293 girls [48.3%]; median age, 26 days [IQR, 10-67 days]) undergoing gene panel screening, only 13 (2.1%; 95% CI, 1.0%-3.3%) resulted in potential childhood-onset diagnoses, a significantly lower rate than those screened by genome sequencing (P < .001).In this case series study, genome sequencing as a proactive screening approach for children, due to its unrestrictive gene content and technical advantages in comparison with an exome-based gene panel for medically actionable childhood conditions, uncovered a wide range of heterogeneous high-penetrance pediatric conditions that could guide early interventions and medical management.
Association Between Gestational Age and Academic Achievement of Children Born at Term
Authors: George L. Wehby
Journal: JAMA Network Open (2023)

Importance Differences in academic achievement by gestational age of children born at term, especially at 39 to 41 weeks, are not well understood. Objective To examine differences in academic achievement among children born between 37 and 41 weeks’ gestational age. Design, Setting, and Participants This retrospective cohort study linked birth certificates of children born in Iowa from 1989 to 2009 with school test scores for grades 2 to 11 from 2017 to 2018. Statistical analysis was performed from January to March 2023. Exposures Gestational age at 37, 38, 39, and 41 weeks vs 40 weeks from clinical or obstetric and calendar measures. Main Outcomes and Measures Outcomes were scores in national percentile rankings (NPRs) on standardized school tests in math and reading. Covariates included demographic and prenatal risk factors. Results The sample included 536 996 children (50.7% male children and 49.3% female children) with math scores (3 576 045 child-grade observations; 6.6%, 15.7%, 28.6%, 35.5%, and 13.7% born at 37, 38, 39, 40, and 41 weeks, respectively) and 537 078 children with reading scores (3 590 408 child-grade observations). Score differences for those born at 39 vs 40 weeks were −0.028 NPRs (95% CI, −0.18 to 0.12 NPRs) for math and 0.085 NPRs (95% CI, −0.067 to 0.24 NPRs) for reading using the clinical or obstetric measure and 0.03 NPRs (95% CI, −0.14 to 0.20 NPRs) for math and 0.13 NPRs (95% CI, −0.042 to 0.31 NPRs) for reading using the calendar measure. With the clinical or obstetric measure, score differences between those born at 41 and 40 weeks were 0.19 NPRs (95% CI, −0.0052 to 0.38 NPRs) for math and 0.098 NPRs (95% CI, −0.096 to 0.29 NPRs) for reading. With the calendar measure, score differences for those born at 41 weeks were −0.22 NPRs (95% CI, −0.43 to −0.013 NPRs) for math and −0.28 NPRs (95% CI, −0.49 to −0.074 NPRs) for reading. With the clinical or obstetric measure, score differences between those born at 37 and 38 weeks vs 40 weeks were −0.59 NPRs (95% CI, −0.84 to −0.33 NPRs) and −0.44 NPRs (95% CI, −0.62 to −0.26 NPRs), respectively, for math, and −0.066 NPRs (95% CI, −0.32 to 0.19 NPRs) and −0.19 NPRs (95% CI, −0.37 to 0.0038 NPRs), respectively, for reading. Conclusions and Relevance This study suggests that there is no evidence of a difference in math and reading scores over grades 2 to 11 among children born between 39 and 40 weeks’ gestation, and overall no evidence of better scores among those born at 41 weeks’ gestation compared with 40 weeks’ gestation. The results can further inform decisions on delivery timing at term birth by offering insights into long-term associations of delivery timing with cognitive development and school achievement.
Preterm Prenatal Education—A Novel Approach
Authors: Amelia Q. Schuyler, Waldemar A. Carlo
Journal: JAMA Pediatrics (2023)

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